Role of nitric oxide in myocardial dysfunction after combined burn and smoke inhalation injury

Kazutaka Soejima, Frank C. Schmalstieg, Lilian D. Traber, Csaba Szabo, Andrew Salzman, Daniel L. Traber

    Research output: Contribution to journalArticlepeer-review

    19 Scopus citations


    This study tested the hypothesis that nitric oxide (NO) synthesized from inducible NO synthase (iNOS) is responsible for the cardiac dysfunction observed after burn and smoke inhalation injury. Twelve sheep received 40% third-degree burn and smoke inhalation under halothane anesthesia. The animals were divided into two groups: a MEG group [iNOS was inhibited with mercaptoethylguanidine (MEG), a selective inhibitor of iNOS, n=6] and a control group (n=6). The control group showed a significant increase in NO2-/NO3- (NOx) concentration, metabolite of NO, in plasma after 24 h, whereas the MEG group did not. In the control group, cardiac depression was observed immediately after injury associated with hemoconcentration. Cardiac function returned to a normal level within 6 h following injury. In the control group cardiac dysfunction was observed again after 24 h although the hemoconcentration peaked at 24 h after injury and then began to resolve. In the MEG group, cardiac depression and hemoconcentration were not observed. The present data suggest that cardiac depression seen with this combination injury consists of two phases and that the later phase is mediated by iNOS-NO.

    Original languageEnglish (US)
    Pages (from-to)809-815
    Number of pages7
    Issue number8
    StatePublished - Jan 1 2001


    • Inducible nitric oxide synthase
    • Inflammatory cytokine
    • Mercaptoethylguanidine
    • Peroxynitrite
    • Vascular hyperpermeability

    ASJC Scopus subject areas

    • Surgery
    • Emergency Medicine
    • Critical Care and Intensive Care Medicine

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